A 42-year-old man is discovered unconscious by local police while patrolling in a park. He is unresponsive to stimulation. Syringes were found scattered around him. His heart rate is 70/min and respiratory rate is 6/min. Physical examination reveals a disheveled man with track marks on both arms. His glasgow coma scale is 8. Pupillary examination reveals miosis. An ambulance is called and a reversing agent is administered. Which of the following is most accurate regarding the reversal agent most likely administered to this patient?
Q592
A 40-year-old man with alcohol use disorder is brought to the emergency department because of sudden-onset blurry vision, severe upper abdominal pain, and vomiting that started one day after he drank a bottle of paint thinner. Physical examination shows epigastric tenderness without rebound or guarding. Ophthalmologic examination shows a visual acuity of 20/200 bilaterally despite corrective lenses. Arterial blood gas analysis on room air shows:
pH 7.21
Sodium 135 mEq/L
Chloride 103 mEq/L
Bicarbonate 13 mEq/L
An antidote with which of the following mechanisms of action is the most appropriate therapy for this patient's condition?
Q593
A 36-year-old man is brought to the emergency department by a neighbor with signs of altered mental status. He was found 6 hours ago stumbling through his neighbor's bushes and yelling obscenities. The neighbor helped him home, but found him again 1 hour later slumped over on his driveway in a puddle of vomit. He is oriented to self, but not to place or time. His vitals are as follows: temperature, 36.9°C (98.5°F); pulse, 82/min; respirations, 28/min; and blood pressure, 122/80 mm Hg. Cardiopulmonary examination indicates no abnormalities. He is unable to cooperate for a neurological examination. Physical examination reveals muscle spasms involving his arms and jaw. Laboratory studies show:
Na+ 140 mEq/L
K+ 5.5 mEq/L
CI- 101 mEq/L
HCO3- 9 mEq/L
Urea nitrogen 28 mg/dL
Creatinine 2.3 mg/dL
Glucose 75 mg/dL
Calcium 7.2 mg/dL
Osmolality 320 mOsm/kg
The calculated serum osmolality is 294 mOsm/kg. The arterial blood gas shows a pH of 7.25 and a lactate level of 3.2 mmol/L. Urine examination shows oxalate crystals and the absence of ketones. What is the most appropriate treatment indicated for this patient experiencing apparent substance toxicity?
Q594
A 48-year-old woman presents to her family practitioner complaining of tremulousness of both hands for the past few years that have deteriorated over the past 7 months. She sometimes spills coffee while holding a full cup. She is a receptionist and her symptoms have led to difficulties with typing at work. She denies weight loss, diarrhea, fatigue, blurring of vision, walking difficulties, and heat intolerance. The past medical history is significant for well-controlled bronchial asthma. She does not smoke or use illicit drugs, but she drinks one cup of coffee daily. She drinks alcohol only socially and has noticed a decrease in her tremors afterward. She reports that her father had a head tremor, and her mother had hyperthyroidism. The patient is oriented to person, place, time and situation. On physical examination, the eye movements are normal and there is no nystagmus. She has a prominent rhythmic tremor of both hands that increase when hands are stretched with abducted fingers. The muscle strength, tone, and deep tendon reflexes are normal in all 4 limbs. The sensory examination and gait are normal. The laboratory test results are as follows:
Hemoglobin 14.8 g/dL
Leukocytes 5,500/mm3
Platelets 385,000/mm3
BUN 18 mg/dL
Creatinine 0.9 mg/dL
Na+ 143 mmol/L
K+ 4.2 mmol/L
Which of the following is the most appropriate management for this patient?
Q595
A 65-year-old male with a history of hypertension presents to his primary care physician complaining of multiple episodes of chest pain, palpitations, and syncope. Episodes have occurred twice daily for the last week, and he is asymptomatic between episodes. Electrocardiogram reveals a narrow-complex supraventricular tachycardia. He is treated with diltiazem. In addition to its effects on cardiac myocytes, on which of the following channels and tissues would diltiazem also block depolarization?
Q596
A 29-year-old woman presents with low mood and tearfulness on most days for the past 4 weeks. She says that she has been struggling to cope with her life and feels that everything that is going wrong is her fault. She also says that there are nights when she cries herself to sleep as the burden of the whole day is too overwhelming for her. In the last 3 weeks, she cannot recall a day when she felt interested in going out and participating in her daily activities. She also says she doesn’t seem to have much energy and feels fatigued all day. She has lost her appetite and feels that she is losing weight. Over the past month, she also reports experiencing frequent and often unbearable migraine headaches. No significant past medical history. The patient has prescribed a drug for her symptoms which is known to be cardiotoxic and may result in ECG changes. Which of the following is the mechanism of action of the drug most likely prescribed to this patient?
Q597
A 59-year-old man presents to a clinic with exertional chest pain for the past several months. He says the pain is central in his chest and relieved with rest. The physical examination is unremarkable. An electrocardiogram is normal, but an exercise tolerance test revealed ST-segment depression in chest leads V1-V4. He is prescribed nitroglycerin to be taken in the first half of the day. Which of the following statements best describes the reason behind the timing of this medication?
Q598
A 58-year-old male presents to his primary care physician for a check-up. He reports that he visited an urgent care clinic last week for seasonal allergies; he was instructed at that encounter to follow-up with his primary care doctor because his blood pressure measured at that time was 162/88. He denies any bothersome symptoms and reports that he feels well overall. The patient denies any past history of medical problems other than cholecystitis that was surgically treated over 30 years ago. On further probing through review of symptoms, the patient reports that he often feels 'shaky' when performing tasks; he reports that his hands shake whenever he attempts to eat or drink something and also when he writes. Vital signs obtained at the visit are as follows: T 37.2 C, HR 88, BP 154/96, RR 20, SpO2 98%. A second blood pressure reading 10 minutes after the first set of vitals shows a blood pressure of 150/94. Physical examination is overall unremarkable and does not reveal a resting tremor in either hand; however, when the patient is asked to pick up a pen to fill out insurance paperwork, you note a fine shaking in his right hand. Which of the following is the next best step in the management of this patient?
Q599
A primary care physician who focuses on treating elderly patients is researching recommendations for secondary prevention. She is particularly interested in recommendations regarding aspirin, as she has several patients who ask her if they should take it. Of the following, which patient should be started on lifelong aspirin as monotherapy for secondary prevention of atherosclerotic cardiovascular disease?
Q600
A 34-year-old man comes to the physician because of palpitations, shortness of breath, diarrhea, and abdominal cramps for 2 months. Physical examination shows cutaneous flushing of the face. Auscultation of the chest shows bilateral wheezing. A 24-hour urine collection shows increased 5-hydroxyindoleacetic acid (5-HIAA) concentration. A contrast-enhanced CT scan of the abdomen shows an intestinal tumor with extensive metastasis to the liver. A diagnosis of an inoperable disease is made and the patient is started on treatment with octreotide. Six weeks later, the patient's symptoms have improved except for his abdominal pain and frequent loose stools. The physician suggests enrolling the patient in a trial to test additional treatment with a new drug that has been shown to improve symptoms in other patients with the same condition. The expected beneficial effect of this new drug is most likely caused by inhibition of which of the following?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 591: A 42-year-old man is discovered unconscious by local police while patrolling in a park. He is unresponsive to stimulation. Syringes were found scattered around him. His heart rate is 70/min and respiratory rate is 6/min. Physical examination reveals a disheveled man with track marks on both arms. His glasgow coma scale is 8. Pupillary examination reveals miosis. An ambulance is called and a reversing agent is administered. Which of the following is most accurate regarding the reversal agent most likely administered to this patient?
A. Works on dopamine receptors
B. Has a short half-life
C. Can be given per oral
D. Results in acute withdrawal (Correct Answer)
E. Is a non-competitive inhibitor
Explanation: ***Results in acute withdrawal***
- The patient's presentation (unconscious, track marks, miosis, bradypnea) is characteristic of **opioid overdose**. The reversal agent, **naloxone**, rapidly displaces opioids from their receptors, leading to an abrupt onset of withdrawal symptoms.
- **Acute opioid withdrawal** can manifest with symptoms like nausea, vomiting, diarrhea, muscle cramps, and agitation, as the body suddenly lacks the opioid-induced suppression.
- This is the **most clinically significant** characteristic of naloxone in the acute overdose setting, as it explains the immediate physiological response patients experience.
*Works on dopamine receptors*
- **Naloxone** primarily acts as an **opioid receptor antagonist**, particularly at the mu-opioid receptor.
- It does not significantly interact with or exert its primary effects through **dopamine receptors**.
*Has a short half-life*
- While this statement is **factually true** (naloxone has a half-life of 30-81 minutes), it describes a **pharmacokinetic property** rather than a characteristic of its reversal mechanism.
- The question asks about the reversal agent in the context of immediate administration, where the **acute precipitation of withdrawal** is the most defining and immediate clinical consequence.
- The short half-life is clinically relevant for monitoring (patients may re-sedate), but it is not the most accurate statement regarding what happens when the reversal agent is administered.
*Can be given per oral*
- Although **naloxone** can be administered orally, its **bioavailability via the oral route is very low** (less than 3%) due to extensive first-pass metabolism.
- For acute overdose reversal, it is typically administered via intravenous, intramuscular, subcutaneous, or intranasal routes for rapid and effective absorption.
*Is a non-competitive inhibitor*
- **Naloxone** is a **competitive antagonist** of opioid receptors, meaning it competes with opioids for binding sites.
- It does not bind to an allosteric site to reduce the opioid's efficiency (non-competitive inhibition); rather, it directly blocks the receptor.
Question 592: A 40-year-old man with alcohol use disorder is brought to the emergency department because of sudden-onset blurry vision, severe upper abdominal pain, and vomiting that started one day after he drank a bottle of paint thinner. Physical examination shows epigastric tenderness without rebound or guarding. Ophthalmologic examination shows a visual acuity of 20/200 bilaterally despite corrective lenses. Arterial blood gas analysis on room air shows:
pH 7.21
Sodium 135 mEq/L
Chloride 103 mEq/L
Bicarbonate 13 mEq/L
An antidote with which of the following mechanisms of action is the most appropriate therapy for this patient's condition?
A. Inhibition of acetyl-CoA synthetase
B. Inhibition of acetaldehyde dehydrogenase
C. Activation of acetaldehyde dehydrogenase
D. Activation of acetyl-CoA synthetase
E. Inhibition of alcohol dehydrogenase (Correct Answer)
Explanation: ***Inhibition of alcohol dehydrogenase***
- The patient's symptoms (sudden-onset blurry vision, severe abdominal pain, vomiting) and the history of drinking paint thinner (which contains **methanol**) point to **methanol poisoning**.
- **Fomepizole** acts by **inhibiting alcohol dehydrogenase**, which is the enzyme responsible for metabolizing methanol into toxic metabolites like **formic acid**, thus preventing further damage.
*Inhibition of acetyl-CoA synthetase*
- This mechanism is not directly relevant to methanol poisoning treatment.
- **Acetyl-CoA synthetase** is involved in fatty acid metabolism, and its inhibition would not counteract the toxic effects of methanol.
*Inhibition of acetaldehyde dehydrogenase*
- This is the mechanism of action of **disulfiram**, used to treat chronic alcoholism by causing an unpleasant reaction to alcohol consumption.
- It would **increase acetaldehyde levels**, which are not the primary toxins in methanol poisoning.
*Activation of acetaldehyde dehydrogenase*
- While activation of acetaldehyde dehydrogenase would reduce acetaldehyde levels, this is not the therapeutic goal in methanol poisoning.
- The primary toxic metabolites in methanol poisoning are **formic acid**, not acetaldehyde.
*Activation of acetyl-CoA synthetase*
- This mechanism is not involved in the treatment for methanol poisoning.
- Activating this enzyme would not prevent the formation of toxic methanol metabolites.
Question 593: A 36-year-old man is brought to the emergency department by a neighbor with signs of altered mental status. He was found 6 hours ago stumbling through his neighbor's bushes and yelling obscenities. The neighbor helped him home, but found him again 1 hour later slumped over on his driveway in a puddle of vomit. He is oriented to self, but not to place or time. His vitals are as follows: temperature, 36.9°C (98.5°F); pulse, 82/min; respirations, 28/min; and blood pressure, 122/80 mm Hg. Cardiopulmonary examination indicates no abnormalities. He is unable to cooperate for a neurological examination. Physical examination reveals muscle spasms involving his arms and jaw. Laboratory studies show:
Na+ 140 mEq/L
K+ 5.5 mEq/L
CI- 101 mEq/L
HCO3- 9 mEq/L
Urea nitrogen 28 mg/dL
Creatinine 2.3 mg/dL
Glucose 75 mg/dL
Calcium 7.2 mg/dL
Osmolality 320 mOsm/kg
The calculated serum osmolality is 294 mOsm/kg. The arterial blood gas shows a pH of 7.25 and a lactate level of 3.2 mmol/L. Urine examination shows oxalate crystals and the absence of ketones. What is the most appropriate treatment indicated for this patient experiencing apparent substance toxicity?
A. Ethanol
B. Hydroxocobalamin
C. Fomepizole (Correct Answer)
D. N-acetyl cysteine
E. Methylene blue
Explanation: ***Fomepizole***
- **Fomepizole** is indicated for **ethylene glycol** toxicity, which is strongly suggested by the patient's presentation: **high anion gap metabolic acidosis**, increased **osmolal gap**, elevated **creatinine**, and the presence of **oxalate crystals** in the urine.
- It acts by **inhibiting alcohol dehydrogenase**, preventing the metabolism of ethylene glycol to toxic metabolites like glycolic acid and oxalic acid.
*Ethanol*
- **Ethanol** can be used as an antidote for ethylene glycol poisoning, but **fomepizole** is generally preferred due to its more favorable side effect profile and easier dosing.
- It works by competitively inhibiting **alcohol dehydrogenase**, similar to fomepizole, but requires careful monitoring and often causes sedation.
*Hydroxocobalamin*
- **Hydroxocobalamin** is the antidote for **cyanide poisoning**, which typically presents with severe metabolic acidosis, but lacks the characteristic osmolal gap, renal failure, and oxalate crystals seen here.
- It functions by binding to cyanide to form **cyanocobalamin**, which can then be safely excreted.
*N-acetyl cysteine*
- **N-acetyl cysteine (NAC)** is the antidote for **acetaminophen overdose**, which causes liver damage and a different metabolic profile, usually without an osmolal gap or oxalate crystals.
- NAC replenishes **glutathione**, which is essential for detoxifying acetaminophen metabolites.
*Methylene blue*
- **Methylene blue** is used to treat **methemoglobinemia**, a condition typically caused by certain drugs or toxins that leads to impaired oxygen delivery and cyanosis, which is not suggested by the patient's current symptoms or lab results.
- It acts as a **reducing agent** to convert methemoglobin back to hemoglobin.
Question 594: A 48-year-old woman presents to her family practitioner complaining of tremulousness of both hands for the past few years that have deteriorated over the past 7 months. She sometimes spills coffee while holding a full cup. She is a receptionist and her symptoms have led to difficulties with typing at work. She denies weight loss, diarrhea, fatigue, blurring of vision, walking difficulties, and heat intolerance. The past medical history is significant for well-controlled bronchial asthma. She does not smoke or use illicit drugs, but she drinks one cup of coffee daily. She drinks alcohol only socially and has noticed a decrease in her tremors afterward. She reports that her father had a head tremor, and her mother had hyperthyroidism. The patient is oriented to person, place, time and situation. On physical examination, the eye movements are normal and there is no nystagmus. She has a prominent rhythmic tremor of both hands that increase when hands are stretched with abducted fingers. The muscle strength, tone, and deep tendon reflexes are normal in all 4 limbs. The sensory examination and gait are normal. The laboratory test results are as follows:
Hemoglobin 14.8 g/dL
Leukocytes 5,500/mm3
Platelets 385,000/mm3
BUN 18 mg/dL
Creatinine 0.9 mg/dL
Na+ 143 mmol/L
K+ 4.2 mmol/L
Which of the following is the most appropriate management for this patient?
A. Reassurance
B. Primidone (Correct Answer)
C. Levodopa/Carbidopa
D. Clonazepam
E. Propranolol
Explanation: ***Primidone***
- This patient's symptoms are highly suggestive of **essential tremor**, characterized by **bilateral action tremor** that improves with alcohol and has a family history.
- **Primidone**, a **barbiturate derivative**, is a first-line treatment for essential tremor, especially when propranolol is contraindicated or ineffective, as it helps to reduce tremor amplitude.
*Reassurance*
- While reassurance might be appropriate for benign conditions without significant impact on daily life, this patient's tremors are causing **functional impairment** (spilling coffee, difficulty typing) and have progressive worsening.
- A treatable cause has been identified, and therefore, medical management is warranted rather than just reassurance.
*Levodopa/Carbidopa*
- **Levodopa/carbidopa** is the primary treatment for **Parkinson's disease**, which typically presents with a **resting tremor**, bradykinesia, rigidity, and postural instability.
- This patient exhibits an **action tremor**, not a resting tremor, and lacks other parkinsonian features, making levodopa/carbidopa an inappropriate choice for their condition.
*Clonazepam*
- **Clonazepam**, a benzodiazepine, can be used for various tremor disorders, but it is typically reserved for tremors associated with **anxiety** or as an **adjunct therapy** for essential tremor when other first-line agents fail.
- It is not considered a first-line agent for essential tremor and carries risks of dependency and sedation, especially in patients with a history of asthma.
*Propranolol*
- **Propranolol** is generally considered a **first-line treatment** for essential tremor due to its efficacy in reducing tremor amplitude.
- However, the patient has a history of **well-controlled bronchial asthma**, and propranolol, a non-selective beta-blocker, is **relatively contraindicated** in asthma due to the risk of bronchospasm.
Question 595: A 65-year-old male with a history of hypertension presents to his primary care physician complaining of multiple episodes of chest pain, palpitations, and syncope. Episodes have occurred twice daily for the last week, and he is asymptomatic between episodes. Electrocardiogram reveals a narrow-complex supraventricular tachycardia. He is treated with diltiazem. In addition to its effects on cardiac myocytes, on which of the following channels and tissues would diltiazem also block depolarization?
A. L-type Ca channels in skeletal muscle
B. T-type Ca channels in bone
C. P-type Ca channels in Purkinje fibers
D. N-type Ca channels in the peripheral nervous system
E. L-type Ca channels in smooth muscle (Correct Answer)
Explanation: ***L-type Ca channels in smooth muscle***
- **Diltiazem** is a **calcium channel blocker** that acts on **L-type calcium channels**, which are extensively found in both cardiac muscle and vascular **smooth muscle**.
- By blocking these channels in smooth muscle, diltiazem induces **vasodilation**, contributing to its use in hypertension, as seen in the patient's history.
*L-type Ca channels in skeletal muscle*
- While skeletal muscle does contain L-type calcium channels (also known as dihydropyridine receptors), their primary role is in **excitation-contraction coupling**, acting as voltage sensors rather than directly regulating calcium influx for contraction.
- **Skeletal muscle contraction** is primarily triggered by calcium release from the sarcoplasmic reticulum, not direct calcium influx through L-type channels, making them largely **insensitive to calcium channel blockers** like diltiazem at therapeutic doses.
*T-type Ca channels in bone*
- **T-type calcium channels** are found in various tissues, including neurons and cardiac pacemaker cells, but they are generally **not the primary target of diltiazem**, which preferentially binds to L-type channels.
- Furthermore, **bone tissue** is not known to have a significant physiological role mediated by T-type calcium channels that would be relevant to diltiazem's action or clinical effects.
*P-type Ca channels in Purkinje fibers*
- **Purkinje fibers** primarily rely on **L-type calcium channels** for phase 2 of their action potential and are sensitive to diltiazem, but **P-type calcium channels** are mainly found in neurons.
- P-type calcium channels are involved in **neurotransmitter release** at the presynaptic terminal, and diltiazem does not typically block these channels clinically.
*N-type Ca channels in the peripheral nervous system*
- **N-type calcium channels** are predominantly located in the **peripheral and central nervous systems**, where they are crucial for **neurotransmitter release** at nerve terminals.
- Diltiazem's primary mechanism of action is on **L-type calcium channels**, and it has **minimal to no clinically significant effect** on N-type calcium channels.
Question 596: A 29-year-old woman presents with low mood and tearfulness on most days for the past 4 weeks. She says that she has been struggling to cope with her life and feels that everything that is going wrong is her fault. She also says that there are nights when she cries herself to sleep as the burden of the whole day is too overwhelming for her. In the last 3 weeks, she cannot recall a day when she felt interested in going out and participating in her daily activities. She also says she doesn’t seem to have much energy and feels fatigued all day. She has lost her appetite and feels that she is losing weight. Over the past month, she also reports experiencing frequent and often unbearable migraine headaches. No significant past medical history. The patient has prescribed a drug for her symptoms which is known to be cardiotoxic and may result in ECG changes. Which of the following is the mechanism of action of the drug most likely prescribed to this patient?
A. Acts as an antagonist at the dopamine and serotonin receptors
B. Inhibits the uptake of serotonin and norepinephrine at the presynaptic terminal (Correct Answer)
C. Blocks the reuptake of serotonin, increasing its concentration in the synaptic cleft
D. Non-selectively inhibits monoamine oxidase A and B
E. Stimulates the release of norepinephrine and dopamine in the presynaptic terminal
Explanation: ***Inhibits the uptake of serotonin and norepinephrine at the presynaptic terminal***
- The patient's symptoms are severely suggestive of **Major Depressive Disorder (MDD)**, which is often treated with **tricyclic antidepressants (TCAs)** in cases of severe depression or when other agents are ineffective. TCAs work by **inhibiting the reuptake of both serotonin and norepinephrine**.
- TCAs are known for their potential **cardiotoxicity**, including **ECG changes** such as QT prolongation, due to their inhibition of fast sodium channels. The patient's severe Migraine headaches are also a specific indication for some TCAs, such as **amitriptyline**.
*Acts as an antagonist at the dopamine and serotonin receptors*
- Medications that act as antagonists at dopamine and serotonin receptors are typically **antipsychotics**, used to treat conditions like schizophrenia or bipolar disorder, which do not align with the patient's symptoms.
- While some antipsychotics can have cardiac side effects, their primary mechanism is not for MDD with this symptom constellation and known cardiotoxicity profile.
*Blocks the reuptake of serotonin, increasing its concentration in the synaptic cleft*
- This describes the mechanism of **Selective Serotonin Reuptake Inhibitors (SSRIs)**. SSRIs are generally first-line for depression but are less likely to cause the severe cardiotoxicity and ECG changes mentioned.
- While effective for depression, SSRIs are not typically associated with being "cardiotoxic and may result in ECG changes" to the same extent as TCAs.
*Non-selectively inhibits monoamine oxidase A and B*
- This describes the mechanism of **non-selective monoamine oxidase inhibitors (MAOIs)**. While MAOIs are effective antidepressants, they are typically reserved for **refractory depression** due to significant drug and food interactions.
- Although MAOIs can have cardiovascular side effects (e.g., hypertensive crisis), their profile of cardiotoxicity is different from what is described, and they are usually not a first-line choice for general severe depression unless other options have failed.
*Stimulates the release of norepinephrine and dopamine in the presynaptic terminal*
- This mechanism is characteristic of **stimulants** (e.g., amphetamines) or some atypical antidepressants like **bupropion**, which also inhibit reuptake. Stimulants are used for conditions like ADHD and narcolepsy, not primary MDD with these specific features.
- While some stimulants can have cardiovascular effects, they are not typically described as cardiotoxic with specific ECG changes in the context of treating severe depression.
Question 597: A 59-year-old man presents to a clinic with exertional chest pain for the past several months. He says the pain is central in his chest and relieved with rest. The physical examination is unremarkable. An electrocardiogram is normal, but an exercise tolerance test revealed ST-segment depression in chest leads V1-V4. He is prescribed nitroglycerin to be taken in the first half of the day. Which of the following statements best describes the reason behind the timing of this medication?
A. To prevent methemoglobinemia
B. More effective in patients with angina due to anemia
C. To avoid nitrate tolerance (Correct Answer)
D. To prevent collapse
E. To avoid nitrate headache
Explanation: ***To avoid nitrate tolerance***
- Chronic or continuous exposure to nitrates leads to **nitrate tolerance**, where therapeutic effectiveness diminishes over time.
- A **nitrate-free interval** (typically 10-14 hours, such as overnight or during the latter half of the day) allows restoration of nitrate sensitivity and maintains therapeutic efficacy.
- This is the primary reason for timing nitrate administration to the first half of the day.
*To prevent methemoglobinemia*
- **Methemoglobinemia** is a rare, dose-related complication typically seen with nitrate overdose or very high doses, not standard therapeutic use.
- The timing of nitroglycerin administration is not designed to prevent this rare adverse effect.
*More effective in patients with angina due to anemia*
- This statement is **not medically accurate**. Nitroglycerin timing is unrelated to whether angina is caused by anemia or coronary artery disease.
- Anemia-related angina is managed by correcting the underlying anemia, and nitrate efficacy does not vary based on anemia status.
*To prevent collapse*
- While nitroglycerin can cause **hypotension** and potential syncope due to vasodilation, this is an acute effect managed by dose titration and patient education.
- The nitrate-free interval strategy addresses **tolerance prevention**, not acute hemodynamic side effects.
*To avoid nitrate headache*
- **Nitrate-induced headache** is a common acute side effect caused by cerebral vasodilation, typically occurring shortly after administration.
- The timing strategy (nitrate-free interval) is designed to prevent tolerance, not to avoid this acute side effect, which usually diminishes with continued use.
Question 598: A 58-year-old male presents to his primary care physician for a check-up. He reports that he visited an urgent care clinic last week for seasonal allergies; he was instructed at that encounter to follow-up with his primary care doctor because his blood pressure measured at that time was 162/88. He denies any bothersome symptoms and reports that he feels well overall. The patient denies any past history of medical problems other than cholecystitis that was surgically treated over 30 years ago. On further probing through review of symptoms, the patient reports that he often feels 'shaky' when performing tasks; he reports that his hands shake whenever he attempts to eat or drink something and also when he writes. Vital signs obtained at the visit are as follows: T 37.2 C, HR 88, BP 154/96, RR 20, SpO2 98%. A second blood pressure reading 10 minutes after the first set of vitals shows a blood pressure of 150/94. Physical examination is overall unremarkable and does not reveal a resting tremor in either hand; however, when the patient is asked to pick up a pen to fill out insurance paperwork, you note a fine shaking in his right hand. Which of the following is the next best step in the management of this patient?
A. Referral to a neurologist
B. Instruction to begin a diet and exercise regimen
C. Initiate levodopa
D. Start propranolol (Correct Answer)
E. Prescribe losartan
Explanation: ***Start propranolol***
- This patient presents with an **action tremor** that is worsened with activity, consistent with **essential tremor**. Propranolol, a **beta-blocker**, is a first-line treatment for essential tremor, especially given the patient's concomitant **hypertension**.
- The patient's blood pressure readings (154/96 and 150/94 mmHg) indicate **Stage 2 hypertension**, which also needs to be managed. Propranolol effectively treats both the tremor and helps in lowering blood pressure.
*Referral to a neurologist*
- While a neurologist might be consulted for complex or unclear tremor cases, initiating first-line treatment for a clear case of **essential tremor** with co-occurring **hypertension** is appropriate for a primary care physician.
- Referral is usually considered if the tremor is **atypical**, refractory to initial treatment, or if there's suspicion of other neurological conditions.
*Instruction to begin a diet and exercise regimen*
- **Lifestyle modifications** are important for managing hypertension and overall health, but they specifically do not address the patient's bothersome **essential tremor**.
- While beneficial as an adjunct, **diet and exercise** alone are insufficient to manage either the tremor or the blood pressure to target levels in this case.
*Initiate levodopa*
- **Levodopa** is the primary treatment for **Parkinson's disease**, which typically presents with a **resting tremor**, bradykinesia, rigidity, and postural instability.
- This patient's tremor is an **action tremor**, not a resting tremor, making Parkinson's disease less likely and levodopa an inappropriate choice.
*Prescribe losartan*
- **Losartan** is an **ARB (angiotensin receptor blocker)** used for hypertension, which would effectively treat the patient's elevated blood pressure.
- However, losartan would **not address the essential tremor**, and propranolol offers the advantage of treating both conditions simultaneously.
Question 599: A primary care physician who focuses on treating elderly patients is researching recommendations for secondary prevention. She is particularly interested in recommendations regarding aspirin, as she has several patients who ask her if they should take it. Of the following, which patient should be started on lifelong aspirin as monotherapy for secondary prevention of atherosclerotic cardiovascular disease?
A. An 83-year-old female with a history of a hemorrhagic stroke 1 year ago without residual deficits
B. A 75-year-old male who had a drug-eluting coronary stent placed 3 days ago
C. A 67-year-old female who has diabetes mellitus and atrial fibrillation
D. A 45-year-old female with no health problems
E. A 63-year-old male with a history of a transient ischemic attack (Correct Answer)
Explanation: **A 63-year-old male with a history of a transient ischemic attack**
- A patient with a history of **Transient Ischemic Attack (TIA)** has a high risk of subsequent stroke and should be on **lifelong aspirin monotherapy** for secondary prevention of **atherosclerotic cardiovascular disease (ASCVD)**.
- Aspirin helps prevent further thrombotic events by inhibiting platelet aggregation, making it a cornerstone for secondary prevention after TIA or ischemic stroke.
*An 83-year-old female with a history of a hemorrhagic stroke 1 year ago without residual deficits*
- Aspirin is generally **contraindicated** in patients with a history of **hemorrhagic stroke** due to the increased risk of recurrent bleeding.
- In such cases, the risks of aspirin therapy typically **outweigh the benefits** for cardiovascular prevention.
*A 75-year-old male who had a drug-eluting coronary stent placed 3 days ago*
- A patient with a recently placed **drug-eluting stent (DES)** requires **dual antiplatelet therapy (DAPT)**, typically aspirin plus a P2Y12 inhibitor, for a specific duration (e.g., 6-12 months), not aspirin monotherapy.
- Monotherapy with aspirin alone would be **insufficient** to prevent stent thrombosis in the immediate post-stenting period.
*A 67-year-old female who has diabetes mellitus and atrial fibrillation*
- This patient has two significant risk factors requiring specific management: **diabetes mellitus** for cardiovascular risk and **atrial fibrillation** for stroke risk.
- For atrial fibrillation, **anticoagulation with warfarin or a direct oral anticoagulant (DOAC)** is typically indicated, which makes aspirin monotherapy either unnecessary or potentially harmful if used alone.
*A 45-year-old female with no health problems*
- There is no indication for **aspirin primary prevention** in this patient, especially given the increased risk of bleeding without a clear cardiovascular benefit.
- Guidelines currently recommend against routine aspirin use for primary prevention in healthy individuals due to the **unfavorable risk-benefit ratio**.
Question 600: A 34-year-old man comes to the physician because of palpitations, shortness of breath, diarrhea, and abdominal cramps for 2 months. Physical examination shows cutaneous flushing of the face. Auscultation of the chest shows bilateral wheezing. A 24-hour urine collection shows increased 5-hydroxyindoleacetic acid (5-HIAA) concentration. A contrast-enhanced CT scan of the abdomen shows an intestinal tumor with extensive metastasis to the liver. A diagnosis of an inoperable disease is made and the patient is started on treatment with octreotide. Six weeks later, the patient's symptoms have improved except for his abdominal pain and frequent loose stools. The physician suggests enrolling the patient in a trial to test additional treatment with a new drug that has been shown to improve symptoms in other patients with the same condition. The expected beneficial effect of this new drug is most likely caused by inhibition of which of the following?
A. Histidine decarboxylase
B. Plasma kallikrein
C. Vasoactive intestinal peptide
D. Tryptophan hydroxylase (Correct Answer)
E. Dopamine β-hydroxylase
Explanation: ***Tryptophan hydroxylase***
- This patient presents with symptoms consistent with **carcinoid syndrome** from an intestinal neuroendocrine tumor with liver metastases. The increased urinary **5-HIAA** confirms serotonin overproduction.
- While existing treatment with **octreotide** (a somatostatin analog) controls most symptoms, persistent abdominal pain and diarrhea suggest continued serotonin effects. A new drug targeting **tryptophan hydroxylase** would inhibit the rate-limiting step in serotonin synthesis, thus reducing serotonin levels.
*Histidine decarboxylase*
- This enzyme converts **histidine to histamine**. While histamine can contribute to flushing in some carcinoid tumors, it is not the primary mediator of the systemic symptoms in this case.
- The main issue here is serotonin overproduction, not histamine.
*Plasma kallikrein*
- **Plasma kallikrein** is involved in the kinin-kallikrein system, which produces **bradykinin**, a potent vasodilator. While bradykinin can cause flushing, it is not primarily responsible for the GI symptoms or serotonin overproduction seen in carcinoid syndrome.
- Inhibiting plasma kallikrein would not address the fundamental problem of excess serotonin.
*Vasoactive intestinal peptide*
- **VIP (Vasoactive Intestinal Peptide)** is a neuroendocrine peptide that can cause watery diarrhea and flushing, often associated with **VIPomas**.
- However, the patient's elevated **5-HIAA** strongly points towards serotonin overproduction from a carcinoid tumor, not a VIPoma.
*Dopamine β-hydroxylase*
- This enzyme converts **dopamine to norepinephrine**. This pathway is relevant to catecholamine synthesis, not serotonin.
- This enzyme would be targeted in conditions involving excess catecholamines (e.g., pheochromocytoma), which is not the case here.